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Nutrition As a Mediator of Oxidative Stress in Metabolic And 176:2 E Diamanti-Kandarakis Nutrition and oxidative stress 176:2 R79–R99 Review and others MECHANISMS IN ENDOCRINOLOGY Nutrition as a mediator of oxidative stress in metabolic and reproductive disorders in women Evanthia Diamanti-Kandarakis1, Olga Papalou1, Eleni A Kandaraki2 and Georgia Kassi2 Correspondence should be addressed 1 2 Department of Endocrinology and Diabetes Center of Excellence, EUROCLINIC, Athens, Greece and Endocrine to E Diamanti-Kandarakis Unit, 3rd Department of Internal Medicine, University of Athens Medical School, Athens, Greece Email e.diamanti.kandarakis@ gmail.com Abstract Nutrition can generate oxidative stress and trigger a cascade of molecular events that can disrupt oxidative and hormonal balance. Nutrient ingestion promotes a major inflammatory and oxidative response at the cellular level in the postprandial state, altering the metabolic state of tissues. A domino of unfavorable metabolic changes is orchestrated in the main metabolic organs, including adipose tissue, skeletal muscle, liver and pancreas, where subclinical inflammation, endothelial dysfunction, mitochondrial deregulation and impaired insulin response and secretion take place. Simultaneously, in reproductive tissues, nutrition-induced oxidative stress can potentially violate delicate oxidative balance that is mandatory to secure normal reproductive function. Taken all the above into account, nutrition and its accompanying postprandial oxidative stress, in the unique context of female hormonal background, can potentially compromise normal metabolic and reproductive functions in women and may act as an active mediator of various metabolic and reproductive disorders. European Journal of European Journal European of Endocrinology Endocrinology (2017) 176, R79–R99 Introduction Oxidative metabolism and redox homeostasis have been in the presence of limited antioxidant defenses in the gradually highlighted as an integral part of aerobic life (1). human body (3). Living organisms cannot exist without oxygen; yet under There is an increasing body of evidence showing that unfavorable cellular conditions, oxygen derivatives can oxidative stress lies in the pathophysiological core of a interrupt oxidative equilibrium; damage proteins, lipids plethora of human diseases (4, 5, 6). However, even under and nucleic acids; and compromise cell viability (2). physiological conditions, normal functions of human Hence, oxidative stress was introduced to define the body, such as nutrition, can potentially generate oxidative imbalance between excessive formation of oxidants stress. Macronutrients can be inflammatory and possibly Invited Author’s profile Dr Evanthia Diamanti-Kandarakis is a Professor of Internal Medicine – Endocrinology and Metabolism and the Chairman of the Department of Endocrinology and Diabetes Center of Excellence, EUROCLINIC, Athens, Greece. Her research interests have focused for the last 25 years on clinical, molecular and environmental aspects of metabolic and reproductive abnormalities in polycystic ovarian syndrome. www.eje-online.org © 20120167 European Society of Endocrinology Published by Bioscientifica Ltd. DOI: 10.1530/EJE-16-0616 Printed in Great Britain Downloaded from Bioscientifica.com at 09/26/2021 01:56:54AM via free access 10.1530/EJE-16-0616 Review E Diamanti-Kandarakis Nutrition and oxidative stress 176:2 R80 and others − − pro-oxidant (7). A new term – nutritional or postprandial (O2 ) generating peroxynitrite (ONOO ), which is believed oxidative stress – has been introduced to describe the to be one of the most toxic RNS produced in human body postprandial state of imbalance between the pro-oxidant and can further promote the production of other forms load and the antioxidant defense as a consequence of RNS, such as nitrogen dioxide (·NO2) and dinitrogen of excess or of inadequate supply with nutrients (8). trioxide (N2O3) (16). Postprandial oxidative stress has been closely linked to In addition to the above mentioned pro-oxidants, subclinical inflammation and endothelial dysfunction other molecules that have also been acknowledged to and therefore could be involved in the pathophysiology share truly pro-oxidant and inflammatory properties are of various metabolic and reproductive disturbances (9, 10). AGEs. AGEs, or glycotoxins, constitute a heterogenous group of more than 20 different compounds, derived from Elements of fundamentals of endogenous nonenzymatic glycation of macromolecules, oxidative metabolism as well as from absorbed exogenous sources (17). Upon their formation, AGEs promote ROS and RNS formation, There are two main classes of free radicals or oxidants: via multiple mechanisms (18). Binding of AGEs to their reactive oxygen species (ROS) and reactive nitrogen multiligand receptor for advanced glycation end products species (RNS). ROS derive from molecular oxygen, (RAGE) activates NF-κB, which in turn leads to increased formed upon incomplete reaction of oxygen, including ROS generation, as well as to the activation of NADPH − − superoxide anion (O2 ), hydroxyl radical (OH ) and oxidase (19, 20). singlet oxygen and hydrogen peroxide (H2O2) (11). This Antioxidants are the opposing force of human body activation takes place via different cellular processes to maintain oxidative equilibrium (Fig. 2) (21). They can (Fig. 1) (12). However, mitochondria are considered be divided into two major categories: enzymatic and to be the principal source of ROS. Specifically, in the nonenzymatic. Enzymatic antioxidants constitute innate, mitochondrial electron transport chain (ETC), there is key enzymes that can detoxify excessive ROS and RNS, a tendency for an electron to directly pass to oxygen, including superoxide dismutase (SOD), catalase (CAT) and − generating eventually superoxide (O2 ) (13). glutathione peroxidase (GPx) (22), whereas nonenzymatic RNS are a family of chemical compounds that antioxidants are exogenous and endogenous molecules, derive from nitric oxide (NO) (14). Physiologically, NO such as glutathione, thioredoxin, vitamin C, vitamin A, is synthesized from L-arginine, via the catalytic action vitamin E, selenium (Se) and zinc (Zn), used to terminate of nitric oxide synthase (NOS) and under the presence pro-oxidants (13, 23). European Journal European of Endocrinology of catalytic cofactors, tetrahydrobiopterin (BH4), flavin When overproduction of free radicals cannot be adenine dinucleotide and flavin mononucleotide (FMN) compensated by the powerful antioxidant defense (15). Under certain stimuli, NO reacts with superoxide system of the body, oxidative stress dominates (24) and Figure 1 Molecular pathways of ROS and RNS production and clearance via different enzymatic reactions (BH4, tetrahydrobiopterin; ENOS, endothelial nitric oxide synthase; FAD, flavin adenine dinucleotide; FMN, flavin mononucleotide; GSH, glutathione; GSSG, glutathione disulfide; 2H O2, hydrogen peroxide; NADPH, nicotinamide adenine dinucleotide phosphate; NO, nitric oxide; RNS, reactive nitrogen − species; ROS, reactive oxygen species; O2 : superoxide anion; OH−, hydroxyl radical; ONOO−, peroxynitrite). www.eje-online.org Downloaded from Bioscientifica.com at 09/26/2021 01:56:54AM via free access Review E Diamanti-Kandarakis Nutrition and oxidative stress 176:2 R81 and others literature focusing on how environmental factors acting during early human development can affect the risk for health and disease. Among environmental factors, nutrition as a potent promoter of these intrauterine epigenetic modifications has been extensively studied (34). Specifically, undernutrition in utero and low birth weight, combined with early catch-up growth during infancy has been linked to increased risk for obesity, insulin resistance, cardiovascular disease and reproductive dysregulation in adulthood (35, 36, 37). Likewise, offspring raised in the context of a prenatally rich nutritional environment are at an increased risk for cardiometabolic disorders and compromised fertility later in life (38, 39). Oxidative stress has been proposed as a potential mediator of nutrition-induced epigenetic changes through various experimental models (40). Maternal malnutrition, obesity or obesogenic maternal diet during gestation, but not during postweaning period (41), was associated with increased oxidative stress markers Figure 2 and impaired antioxidant capacity in the offspring, Pro-oxidants and antioxidants represent the ‘yin and yang’ of making them vulnerable to diabetogenic effects (42, 43). human body, as these opposite forces are actually Simultaneously, antioxidant supplementation was complementary, interconnected and give rise to each other accompanied by a significant attenuation of adiposity in (AGEs, advanced glycation end products; H2O2, hydrogen − − − their offspring (44). peroxide; NO , nitroxyl; O2 , superoxide anion; OH , hydroxyl Currently, the majority of evidence regarding the radical; ONOO−, peroxynitrite; RNS, reactive nitrogen species; domain of developmental programming originates from ROS, reactive oxygen species; RSNO, S-nitrosothiol). experimental models, and there is a long way until ROS initiate multiple molecular pathways (12, 25, 26). definitive conclusions be established. However, nutrition European Journal European of Endocrinology This active implication of ROS in multiple molecular during the critical periods of prenatal and perinatal pathways has led scientific society to investigate the role development can induce epigenetic changes, via different of oxidative stress not only in the pathophysiology
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